Take your mother’s ferry: preimplantation embryo development requires maternal karyopherins for nuclear transport
Momal Sharif, … , Laura Detti, Ignatia B. Van den Veyver
Momal Sharif, … , Laura Detti, Ignatia B. Van den Veyver
Published January 17, 2023
Citation Information: J Clin Invest. 2023;133(2):e166279. https://doi.org/10.1172/JCI166279.
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Commentary

Take your mother’s ferry: preimplantation embryo development requires maternal karyopherins for nuclear transport

Abstract

The genetic basis of preimplantation embryo arrest is slowly being unraveled. Recent discoveries point to maternally expressed proteins required for cellular functions before the embryonic genome is activated. In this issue of the JCI, Wang, Miyamoto, et al. suggest a critical role for karyopherin-mediated protein cargo transport between oocyte cytoplasm and nucleus. Defective maternal oocyte–expressed human karyopherin subunit α7 (KPNA7) and mouse KPNA2 fail to bind a critical substrate, ribosomal L1 domain-containing protein 1 (RSL1D1), affecting its transport to the nucleus. As shown in embryos of Kpna2-null females, the consequences are disrupted zygotic genome activation and arrest of development. These findings have important implications for diagnosis and treatment of female infertility.

Authors

Momal Sharif, Laura Detti, Ignatia B. Van den Veyver

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Figure 1

Maternal genetic factors are implicated in oocyte and early embryonic development.

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Maternal genetic factors are implicated in oocyte and early embryonic de...
(A) There are several maternal genetic factors implicated in oocyte development, fertilization, zygotic cleavage, and early embryonic development. The genetic factors are broadly categorized based on their primary phenotypes and developmental defects. KPNA7 is implicated in preimplantation embryo arrest. (B) Karyopherin-mediated protein cargo transport between oocyte cytoplasm and nucleus is essential for proper ZGA. If defective, maternal oocyte–expressed human KPNA7 and its mouse homolog KPNA2 fail to bind RSD1L1, affecting its transport to the nucleus. The consequences are clinical infertility due to disrupted ZGA and early embryonic arrest (reported by Wang et al., ref. 7).